title: Histone deacetylase inhibitor reduces hypertrophic scarring in a rabbit ear model.
abstract: BACKGROUND
  Hypertrophic scars result from excessive collagen deposition at sites of healing dermal wounds and could be functionally and cosmetically problematic. The authors tested the ability of the histone deacetylase inhibitor trichostatin A to reduce hypertrophic scar formation in a rabbit ear model.
  
  
  METHODS
  The authors have developed a reliable rabbit model that results in hypertrophic scarring. Four 1-cm, full-thickness, circular wounds were made on each ear. After the wounds reepithelialized, 0.02% trichostatin A was injected intradermally into the wounds in the treatment group. Expression of collagen I and fibronectin was detected by reverse transcription polymerase chain reaction and Western blot analysis at postoperative day 23. Scar hypertrophy was quantified by measurement of the scar elevation index at postoperative day 45.
  
  
  RESULTS
  Compared with the control group, injection of trichostatin A led to much more normal-appearing scars in the rabbit ear. The scar elevation index at postoperative day 45 was significantly decreased after injection of trichostatin A compared with untreated scars. Furthermore, the authors confirmed the decreased expression of collagen I and fibronectin at postoperative day 23 (after the rabbits had been treated with trichostatin A for 1 week) in the treated scars compared with the control scars according to reverse transcription polymerase chain reaction and Western blot analysis.
  
  
  CONCLUSIONS
  The introduction of trichostatin A can result in the decreased formation of hypertrophic scars in a rabbit ear model, which is corroborated by evidence of decreased collagen I and fibronectin synthesis.
authors.affiliation: Xi'an and Luzhou, People's Republic of China From the Departments of Plastic Surgery and Pathology, Xijing Hospital, Fourth Military Medical University; and the Department of Blood Transfusion, Affiliated Hospital of Luzhou Medical College.
authors.forename: Jian-Sheng
authors.initials: JS
authors.lastname: Diao
authors.forename: Wen-Sen
authors.initials: WS
authors.lastname: Xia
authors.forename: Cheng-Gang
authors.initials: CG
authors.lastname: Yi
authors.forename: Yang
authors.initials: Y
authors.lastname: Yang
authors.forename: Xi
authors.initials: X
authors.lastname: Zhang
authors.forename: Wei
authors.initials: W
authors.lastname: Xia
authors.forename: Mao-Guo
authors.initials: MG
authors.lastname: Shu
authors.forename: Ying-Mei
authors.initials: YM
authors.lastname: Wang
authors.forename: Lin
authors.initials: L
authors.lastname: Gui
authors.forename: Shu-Zhong
authors.initials: SZ
authors.lastname: Guo
mesh_terms: D000818:Animals; D015153:Blotting, Western; D017439:Cicatrix, Hypertrophic / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D024042:Collagen Type I / Q000096:biosynthesis / Q000235:genetics; D004195:Disease Models, Animal; D004427:Ear Diseases / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D004431:Ear, External / Q000293:injuries* / Q000378:metabolism; D005260:Female; D005353:Fibronectins / Q000096:biosynthesis / Q000235:genetics; D005500:Follow-Up Studies; D005786:Gene Expression Regulation / Q000187:drug effects; D056572:Histone Deacetylase Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D006877:Hydroxamic Acids / Q000008:administration & dosage / Q000627:therapeutic use*; D007271:Injections, Intradermal; D008297:Male; D012333:RNA, Messenger / Q000032:analysis; D011817:Rabbits; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016896:Treatment Outcome; D014945:Wound Healing / Q000187:drug effects; D014947:Wounds and Injuries / Q000150:complications / Q000188:drug therapy* / Q000473:pathology
chemical_list: D024042:Collagen Type I; D005353:Fibronectins; D056572:Histone Deacetylase Inhibitors; D006877:Hydroxamic Acids; D012333:RNA, Messenger; C012589:trichostatin A